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Cells repair damage to their outer membranes not by patching them as previously thought, but by using proteins called caveolins to remove the damaged regions by endocytosis.

Genetic mouse models combined with single-cell RNA sequencing reveal the essential role of SRSF2 in directing MyoD progenitors to distinct skeletal muscle domains and controlling their differentiation through the regulation of targeted genes and alternative splicing during skeletal muscle development.

Dynamic early clusters of nodal proteins in peripheral nerves represent a neurofascin-dependent developmental stage of node assembly during myelination that precedes heminode formation.

An endoplasmic reticulum membrane protein regulates synaptic transmission, alcohol sensitivity, and gene expression by controlling the trafficking of a calcium-activated potassium channel.

The transmembrane protein Kit Ligand and the Kit receptor tyrosine kinase are required for synapse function between specific cell types in the mouse cerebellum.

Ultrastructural, biochemical, and behavioral assessments reveal that the Crtap^-/- mouse model of severe, recessive Osteogenesis Imperfecta presents with defects in tendon structure and strength that correlate with severe motor deficits.

A decrease of the type 2 myotonic dystrophy gene product CNBP causes an impairment of polyamine metabolism and locomotor dysfunction that can be reverted with polyamine supplementation.

A novel mechanism links mechanical signals with the molecular YAP and NOTCH signals operating during developmental myogenesis.

Inhibition of Polo-like kinase that has been shown to exhibit antitumor effect unexpectedly disrupts muscle stem cell function, leading to developmental and regenerative failures.

The functional interaction of Na⁺ and K_ATP channels at the intercalated disk of cardiomyocytes depends on Ankyrin G and is clinically relevant since K_ATP channel mutations affect Na⁺ channel expression.